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Immunology Flashcards

1
Q

what reaction is allergy

A

type 1 hypersensitivity

IgE mediated

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2
Q

what is atopy

A

genetic tendency to produce specific IgE abs on exposure to common environmental antigens

tendency to develop IgE sensitisation

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3
Q

what allergic sx do food allergies produce

A

oral itching, tingling, hives
bronchospasm, wheezeing, laryngeal oedema
anaphylaxis

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4
Q

what happens in a type 1 hypersensitivity reaction

A

IgE attaches to Fc epsilon receptors on mast cells

cross linkage of bound specific IgE by allergen -> degranulation of mast cells and the release of inflammatory mediators

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5
Q

what are the pre-formed mediators in mast cell degranulation

A

histamine
tryptase
heparin
rapid release

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6
Q

what are the synthesised mediators in mast cell degranulation

A

leukotrienes
prostaglandins
slow release

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7
Q

how else can mast cells be activated

A

direct binding of radiocontrast dye, opiates to mast cell

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8
Q

what are the 3 cardinal features of acute allergic reactions and what mediates this

A

pruritus
vasodilation and leakage of fluid = hives, angioedema, hypotension
smooth muscle contraction = bronchospasm

HISTAMINE (acts on histamine receptors)

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9
Q

before planning allergy tests what is required for diagnosis of allergy

A

detailed clinical hx

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10
Q

what are the 2 methods of allergy testing

A

skin prick testing

blood tests - allergen specific IgE in serum

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11
Q

contraindications for skin prick testing

A

severe eczema
unable to stop antihistamines
on immune modulatory drugs
young children

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12
Q

what does a positive result mean in the skin prick tests and blood test

A

only confirms IgE sensitisation - may or may not be associated with clinical allergy (sx)

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13
Q

what are the blood test results for allergy measured in

A

kUA/L

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14
Q

what test must not be used as a screening test for allergy?

A

serum total IgE

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15
Q

why is serum tryptase useful for allergy testing

A

marker of mast cell degranulation
high levels after anaphylaxis
has a short half life - blood needs to be taken ASAP

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16
Q

if tryptase levels are chronically elevated what does this indicate

A

mastocytosis

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17
Q

what is the gold standard for allergy testing

A

double bind placebo control challenge

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18
Q

what is the basophil activation test

A

in vitro assay -activate patient basophils upon exposure to allergen and measure with flow cytometry

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19
Q

what is a true food allergy

A

IgE mediated de-granulation of mast cells.

Common food allergens: cow’s milk protein, egg, peanuts, tree nuts, fish, prawns

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20
Q

what is oral allergy syndrome

A

due to cross reacting ‘pan-allergens’ which are found in various members of the plant family (fruits, vegetables, nuts etc).

They are heat labile and destroyed by digestion, hence symptoms are usually limited to the oral cavity.

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21
Q

what is a false food allergy and what causes it

A

direct stimulation of mast cells or histamine ingestion Scombroid fish poisoning (scombrotoxicosis) – Histamine is released by bacterial action (spoilage) on scombroid fish (e.g tuna). Symptoms that mimic an allergic reaction occur
when the spoiled fish containing histamine is consumed.

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22
Q

what is food intolerance

A

adverse reaction to food, with no histamine related symptoms e.g Lactose intolerance, gluten sensitivity

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23
Q

investigations for suspected food allergy

A

base them on clinical hx

specific IgE blood tests or skin prick tests

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24
Q

what is eczema caused by

A

chronic skin condition
associated with filaggrin gene mutations
leads to poor barrier function of skin -> allows IgE sensitisation to aero-allergens and food allergens because of the thinner epidermis

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25
what factors flare up eczema
microbes - infections irritants - chemicals and soap allergens - esp aero-allergens other - temp, foods, stress
26
if someone has a true food allergy and eczema what can happen
eczema can flare up hours after allergic reaction
27
what is chronic spontaenous urticaria? (CSU)
common condition referred inappropriately to the Allergy clinic for ‘allergy testing’ characterised by the spontaneous occurrence of hives (urticaria), swellings (angioedema) or both, with daily or almost daily symptoms for at least 6 weeks NOT IgE mediated
28
how is CSU diagnosed?
appearance and description of skin lesions with detailed clinical history
29
what causes CSU?
``` mast cell degranulation due to acute or chronic infections stress autoimmunity pseudo allergy to food and drugs ```
30
what makes CSU worse
Infections • Stress • Alcohol, caffeine, spices, food additives • Hot showers, hot baths, overheating (duvets in bed) • Tight clothing • Medications Aspirin, Paracetamol, NSAIDS, ACE inhibitor, NB: Herbal/natural products • Soaps, detergents, household products, skin creams and lotions
31
what is autoimmunity
breakdown in the mechanisms that maintain ‘self tolerance’ (elimination of self reactive cells) leads to activation of self reactive clones of B and T cells leads to generation of autoantibodies
32
do healthy individuals produce autoantibodies
yes - they help to remove products of tissue breakdown and clear up cell debris low titre ANA are seen in absence of overt disease
33
what are autoimmune diseases
occurs when humoral and/or cell mediated responses to self antigen are associated with pathological changes
34
what are the 2 types of autoimmune diseases
organ specific | non-organ specific
35
examples of organ specific autoimmune diseases
``` MS Hashimoto's, thyroiditis, thyrotoxicosis myasthenia gravis pernicious anaemia Addison's disease insulin dependent DM ```
36
examples of non-organ specific autoimmune diseases
dermatomyositis SLE scleroderma rheumatoid arthritis
37
what is autoimmune serology
identification and measurement of serum autoantibodies for diagnostic purposes
38
what are the methods of identification for autoantibodies
immunofluorescence, ELISA
39
what can a positive ANA test indicate
connective tissue disease - SLE, Sjorgen's, sclerosis rheumatoid arthritis and autoimmune thyroid disease chronic infectious diseases (mononucleosis, hep C, bacterial endocarditis, TB) drugs - hydralazine, isoniazid, anticonvulsives
40
what disease is associated with IgA Endomysial antibodies, IgA tTG antibodies
coeliac disease
41
what condition are Anti-glomerular basement membrane (GBM) Antibodies associated with
Goodpasture's syndrome
42
what disease is associated with Anti-gastric parietal cell antibodies and Anti-intrinsic factor antibodies
pernicious anaemia
43
what antibodies is microscopic polyangitis associated with
Anti-MPO (p-ANCA)antibodies
44
what antibodies are phospholipid syndrome (Hughes) associated with
anti-cardiolipin antibodies
45
what conditions has Anti SSA (Ro) & Anti SSB(La) antibodies
Sjorgen's syndrome
46
what antibodies are associated with rheumatoid arthritis
Anti- cyclic citrullinated peptide (CCP) antibodies (not rheumatoid factor)
47
clinical presentation of Sjogren's/Sicca syndrome
``` female (50) decrease in secretions dry itchy irritated eyes dry mouth dental problems due to lack of saliva difficulty swallowing joint pain muscle aches low mood irritability impaired concentration fatigue ```
48
clinical presentation of SLE
skin (photosensitivity, rashes), joints (pain and swelling often affecting small joints) and organs (including kidneys, lungs, and brain)
49
clinical presentation of phospholipid syndrome
``` can occur in SLE patients high risk of blood clots recurrent miscarriages arterial/venous thrombosis livedo reticularis thrombocytopenia ```
50
clinical presentation of coeliac disease
``` diarrhoea abdominal pain bloating flatulence associated with type 1 DM dermatitis herpetiformis (blistering on elbows) ```
51
clinical presentation of myasthenia gravis
muscle weakness, commonly affecting muscles controlling the eyes and eyelids, facial expression, chewing, swallowing, and speaking MG may also affect muscles of the arms, legs, neck, and respiratory muscles
52
antibodies associated with granulomatosis with polyangitis (GPA or Wegener's granulomatosis)
Anti-PR3 (c-ANCA) antibodies
53
clinical presentation of GPA or wegener's granulomatosis
flu like sx (prodromal syndrome associated with ENT problems) followed by renal failure
54
what are primary systemic vasculitides
group of clinical disorders characterised by inflammation of blood vessels causing ischaemia and organ damage commonly multi system involvement - as inflammation can involve several vascular beds -> renal failure, pulmonary haemorrhage
55
what investigations are ordered for suspected vasculitis
``` blood test biopsy angiography antibody tests - ANCA, GBM serum cryoglobulins complement ```
56
what are the large vessel vasculitis?
Giant cell arteritis | Takayasu arteritis
57
what are the medium vessel vasculitis?
* Polyarteritis nodosa | * Kawasaki disease
58
how can small vessel vasculitis be categorised
ANCA associated vasculitis | immune complex small vessel vasculitis
59
what are the ANCA associated small vessel vasculitis
Granulomatosis with Polyangiitis (GPA) formerly Wegener’s Granulomatosis Microscopic Polyangiitis (MPA) Eosinophilic Granulomatosis with Polyangiitis (EGPA) formerly Churg- Strauss syndrome
60
what are the immune complex small vessel vasculitis
* Anti-GBM disease (Goodpasture’s syndrome) * Cryoglobulinaemic vasculitis * IgA vasculitis (Henoch-Schonlein) * Hypocomplementaemic urticarial vasculitis
61
which is the most common small vessel vasculitis
Granulomatosis with Polyangiitis (GPA) -formerly ‘Wegener’s granulomatosis
62
what are the 2 forms of granulomatosis with polyangitis
generalised form - pulmonary involvement may manifest as breathlessness; renal involvement manifests as (crescentic) glomerulonephritis localised form - limited to the upper respiratory tract with chronic sinusitis, nasal crusting and/or recurrent epistaxis
63
what is the purpose of immunology testing
aids in clinical diagnosis severity of disease prognosis of disease monitoring - disease activity, treatment, relapse, remission
64
what detection method is used for ANA testing
immunoflourescne or ELISA
65
what additional tests do you perform after positive ANA test
abs to DNA by ELISA (confirms ds-DNA) = crithidia test abs to ENA - SSA (R0), SSB (La), RNP, Sm, Scl-70, Jo-1
66
what are the 2 classes of immune deficiency?
primary and secondary
67
what is primary immune deficiency due to
an immunological defect (usually genetic) very rare
68
what is secondary immune deficiency due to
``` another disease drugs - immunosuppresssants, chemo, steroids myeloma, CLL nephrotic dyndrome AIDS protein losing enteropathy ```
69
what cells make up the innate immune system
neutrophils macrophages complement
70
what cells make up the adaptive immune system
B cells and antibodies | T cells
71
list 5 examples of primary immune deficiency
``` common variable immune deficiency (CVID) C1 esterase inhibitor deficiency/hereditary angioedema (HAE) X-linked agammaglobulinaemia (XLA) severe combined immune deficiency (SCID) chronic granulomatous disease (CGD) ```
72
what are the 6 hallmarks of primary immune deficiency (not HAE)
``` recurrent serious unusually persistent resistant to treatment unusual organisms unusual spread ```
73
what are the 10 warning signs of primary immunodeficiency
1. >=4 new ear infections within 1 year 2. >= 2 serious sinus infections within 1 year 3. >= 2 months of abx with little/no affect 4. >=2 pneumonias per year 5. failure of infant to gain weight or grow normally 6. recurrent, deep skin or organ abscesses 7. persistent thrush in mouth or elsewhere on skin after 1 year of age 8. requires IV abx to clear infections 9. >=2 deep seated infections 10. fhx of primary immune deficiency
74
what pathogens would we expect to see in a T cell defect?
pneumocystis severe fungal/viral infections HIV
75
what pathogens would we expect to see in a B cell or complement defect?
encapsulated bacteria strep pneumoniae haemophilius influenzae
76
what pathogens would we expect to see if neutrophils were defective
staph serratia klebiseilla aspergillus
77
what pathogens would we expect to see if there was complement deficiency only
recurrent neisserial infections | meningitis, gonorrhoea
78
what are patients with primary immune deficiency more predisposed to?
autoimmune diseases (deficiency in one section can lead to overactivity in another) malignancies granulomatous disease
79
what are the 2 complications of diagnosing a primary immune deficiency late
1) irreversible structural damage which can be prevented by early treatment (bronchiectasis, give IV Ig) 2) life threatening laryngeal oedema which can be prevented by appropriate treatment (C1 esterase inhibitor deficiency = hereditary angioedema)
80
what are the initial screening tests for PID?
FBC - total lymphocyte and neutrophil count Serum Igs - IgG, IgA, IgM Complement - C3 & C4
81
what additional tests can be offered after initial screening and history for suspected PID
Specific antibodies to tetanus, haemophilius, pneumococcus (vaccine levels) Lymphocyte subsets (T cells - CD4, CD8) , B cells, NK cells C1 esterase inhibitor NBT test for neutrophil oxidative burst
82
how would someone with common variable deficiency present
problem with abs made - require Ig replacement therapy young adult - male or female recurrent bacterial infections affecting lungs, sinuses, ears has autoimmune diseases - idiopathic thrombocytopenic purpura, autoimmune haemolytic anaemia possible signs of end organ damage such as bronchiectasis
83
what screening test would you request for CVID and what result would you expect
serum immunoglobulins low IgG, low IgA and low/normal IgM
84
what other tests could be requested for suspected CVID diagnosis
IgG subclasses antibodies to haemophilius lymphocyte phenotyping - normal B and T cells normal lymphocyte functioning
85
how does X-linked agammaglobulinaemia present
affects male infants only (as passed on by mother) Recurrent bacterial infections of lungs, ears, gut
86
what are the typical results we would expect to see in someone with X-linked agammaglobulinaemia
low IgG, IgA, IgM low total lymphocyte count low/absent B lymphocytes - problem with the B cells (as very low Igs) normal T lymphocytes BTK gene mutations
87
what is severe combined immunodeficiency
paed medical emergency B and T cell disorder
88
what is the typical presentation for SCID
young infant/baby faltering growth diarrhoea severe candidiasis (fungus)
89
what results would you expect to see in a SCID patient
lymphocyte levels undetectable both B and T cell very low low Igs
90
what age do children get their full levels of Igs?
2 years IgG can be higher though as get them through the placenta from mother and breast milk
91
what is hereditary angioedema and what is it a deficiency in
autosomal dominant condition associated with low plasma levels of the C1 inhibitor leads to uncontrolled release of bradykinin resulting in oedema of tissues C1 esterase inhibitor deficiency there is a defect in complement (innate immune system) - complement has inhibitors as powerful system lack of C1 inhibitor leads to complement always being switched on -> low C4 (being used up)
92
what is the clinical presentation for someone with suspected hereditary angioedema
recurrent, episodic, non-pitting circumscribed oedema (no urticaria) - often mistaken for anaphylaxis in A&E unpredictable acute attacks at any body location - face, larynx, tongue, GIT, GUT, hand or arm, leg or foot
93
what screening tests would you order for hereditary angioedema and what would the results be
complement components C3 & C4 low C4, normal C3 then confirm by requesting C1 esterase inhibitor (see low levels)
94
what is the treatment for hereditary angioedema
C1 esterase inhibitor by infusion
95
what is chronic granulomatous disease
defects in proteins involved in oxidative burst of neutrophils/phagocytes (lack of NADPH oxidase)
96
what is the typical presentation for chronic granulomatous disease
recurrent pneumonias recurrent abscesses due to bacteria and fungi (s aureus, aspergillus, klebsiella) delayed healing leads to oesophageal strictures (see on barium swallow)
97
what test results would we order for chronic granulomatous disease and what results would we expect
FBC - low Hb, normal lymphocytes, elevated neutrophils, elevated ESR Serum Igs elevated Raised CRP Normal neutrophil phagocytosis Absent neutrophil respiratory burst

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